Wednesday, 27 August 2014

The commenter Melanie McSmiley reduced her weight by 45% using something very much like the above diet, and didn't suffer from any horrible side-effects such as Metabolic Shut-down. Well done, Melanie!

Here's an interesting talk by Denise Minger, which contains some big surprises:-

From Further research for consideration in 'the A2 milk case'.
"Prior to discussion it must be clarified that the hypothetical link between A1 consumption with autistic spectral disorder (ASD) and schizophrenia relates not to the cause of the condition but to the aggravation of symptoms associated with these neurological
conditions. More specifically, the hypothesis states that the absorption of food-derived exomorphins such as beta casomorphin 7 (BCM 7) may aggravate symptoms associated with ASD or schizophrenia.

This hypothesis is the basis of 'dietary intervention' that excludes gluten and casein (Knivsberg et al., 2002) from the diet of ASD patients. The former, gluten, has been shown to release gliadamorphin, an exomorphin comparable in opioid activity to BCM-7. A number of laboratories in the United States and Europe offer urine tests, which determine the level of peptides including BCM 7 and other beta casomorphins to serve as an indication of the potential usefulness of dietary intervention in the treatment of ASD patients. One published study reports that a casein- and gluten-free diet was accompanied by improvement in 81% of autistic children within 3 months (Cade et al., 2000)."

According to What is gliadorphin?
"What is gliadorphin? Gliadorphin (also called alpha-gliadin or gluteomorphin) is a substance that resembles morphine. Ordinarily, this is a short-lived by-product from the digestion of gluten molecules (found in wheat, barley, rye, oats, and several other grains). Gliadorphin is very similar to casomorphin. Gliadorphin has been verified by mass spectrometry techniques to be present in unusual quantities in urine samples of children with autism, and are believed by many to be a central part of the system of causes and effects that cause autistic development. The most probable reasons for the presence
of these molecules are:
* One or more errors in the breakdown (digestion) process caused by enzyme deficiency and/or
*
Abnormal permeability of the gut wall (that would allow these relatively large molecules to enter the bloodstream from the intestine in abnormal quantities)."

2. It's much higher in protein (4g/100mL) than human breast milk (1.1g/100mL), as baby cows are supposed to grow very rapidly, unlike baby humans. As 80% of the protein in milk is casein, and casein is joined to calcium as calcium caseinate, this increases the calcium intake, and too much calcium relative to magnesium is constipating. A solution is to increase magnesium intake, or dilute 1 part cow's milk with ~3 parts water & add some coconut oil, to get the fat content back up to 4.4g/100mL.

Friday, 22 August 2014

I don't have anything to say about Yoni Freedhoff's blog post on Myths, Presumptions, and Facts about Obesity, except for Myth 1.
"Small sustained changes in energy intake or expenditure will produce large, long-term weight changes."

This is misleading. One small sustained change (say, -100kcals/day) in energy balance results in one sustained change in weight of -10lbs. If no further changes are made, there are no further changes in weight. However...

If, after the result of the small sustained change has stabilised, another small sustained change (say, -100kcals/day) in energy balance is made, there's another sustained change in weight of -10lbs. And so on...

A series of small sustained changes in energy balance will produce large, long-term weight changes.

Tuesday, 19 August 2014

It's becoming painfully obvious that there's a lot of ignorance about certain dietary "Facts of Life". This post will dispel the myths - backed up by evidence, where necessary.

1. Everyone is Different: This has been a recurring theme on my blog, starting in 2009 with the aptly-named Everyone is Different. What this means in practice, is that:-
a) You can't calculate your Energy Expenditure exactly,using one of those fancy equations (e.g. Harris-Benedict).
b) Weight change is proportional to caloric excess/deficit ± inter-personal variation.

3. Glycaemic Index (GI) has NOTHING to do with calories: A low-GI carbohydrate still has 4kcals/g. GI is a useful hint as to whether a carbohydrate may disturb blood glucose levels, but it isn't as useful as Glycaemic Load (GL = GI x grams of carbohydrate in the serving). Watermelon has a very high GI, but 100g of watermelon contains only ~5g of carbohydrates, so the GL is less than 5 i.e. watermelon is as safe as houses.

4. Exercise DOESN'T burn as many calories as you think: Exercise is for fitness, not weight loss (unless you're a professional sports-person, who can expend 1,000's of kcals a day in training).

5. Weight loss doesn't ALWAYS result in reduced Basal Metabolic Rate: Whether or not Basal Metabolic Rate reduces with weight loss depends on the degree of Adipocyte Hyperplasia that occurred during weight gain. Humongous weight gain, also weight gain in childhood, increases adipocyte hyperplasia, which is protective against developing T2DM, but makes the subsequent loss of significant amounts of FM more difficult.

Non-BB'ers tend to get it the wrong way round. They go on crash diets with insufficient protein intake and lose loads of LBM (which increases weight loss, due to the lower Energy Density of LBM relative to FM). They then eat way too much, gaining weight way too rapidly for much (if any) of it to be LBM, even if they are doing hypertrophy training.

Finally, see http://www.bodyrecomposition.com/. What Lyle McDonald doesn't know about fat loss, general nutrition, muscle mass gain and training fits on a postage stamp. He also explains things in language that the sort of person who reads my blog can understand. Just don't leave a comment asking him a question, that's already been answered elsewhere on his site!

If a diet is high in carbohydrates:-
Which of the above foods are most likely to result in weight gain?
Which of the above foods are most likely to result in weight loss?
Answers on a postcard, please!

What's worse than name-calling? When I defecate science all over my opponents, it makes it difficult for them to respond with refutation. If they are unable to use the top 3 levels of the pyramid, they usually use the 4 levels below that. Until the other day.

Notice how the troll Zahc uses standard baiting practices to "suck me in" to replying to him. He:-
1) Repeats the lie about me cherry-picking 2 studies. Those are the only studies that produced results reaching statistical significance, as all of the other studies had RR ~1, with 95% CI's less than 1 and greater than 1.
2) Makes an irrelevant point about mortality. Siri-Tarino et al & Chowdhury et al are about CHD.
3) Repeats the lie about dairy fat not being protective.
4) Issues a challenge to me to comment on his blog post http://diettrialclaims.blogspot.com/2013/06/is-cholesterol-really-that-important.html I've already commented on Zahc's blog. His blog contains two posts riddled with cholesterol denialism and backed-up by a bunch of cherry-picked studies.
5) Gets aerated over me linking to his comment. Things are about to get worse.

I replied to Zahc's comment.Zahc wrote another comment. He:-
1) Repeats the lie about me cherry-picking 2 studies. Persistent, isn't he?
2) Criticises Dr. Dayspring behind his back, a cowardly thing to do. Zahc has no intention of ever debating Dr. Dayspring, as he knows that Dayspring would destroy his uninformed opinions with data.
3) Issues another challenge to me to make another comment. Luckily, I have this blog, so I don't need to waste any more time debating cholesterol denialists.

Zahc has written another comment. He:-
1) Continues with pointless arguments. Typical troll behaviour.
2) Continues to get confused over basic English. "Uninformed Opinion" wasn't referring to what you wrote in your previous comment, you dumbass. It was referring to what you'd be giving Dr. Dayspring. Jeez!
3) Had my previous comment deleted by Amazon. What was I saying about cowardly behaviour?
4) Continues to insult me, in the vain hope that I might leave another comment answering his points. That ain't ever gonna happen. I'll just leave comments with links to this post, or links to other comments. I know a cholesterol denialist when I see one. I know cherry-picked studies when I see them. I know a shite blog when I see one.

Are we done now, Zahc? I can continue this, ad infinitum. This blog post is all about you (& Allen I. Branson). You're just making yourself look like a total pillock. Have you "debated" with Dr. Dayspring or Dr. Edwards, yet? Somehow, I think not.

Blatant lies are worse than Straw man fallacies, as such fallacies are usually caused by my opponent being ignorant of my argument and confabulating.

Low-carb diets with up to 50%E from fats are fine. There's no Metabolic Advantage to ketogenic diets and there are many disadvantages to long-term ketogenic diets. If you suffer from refractory epilepsy, a medically-supervised ketogenic diet is fine. Branched Chain Amino Acids can be added as adjunctive therapy, as they are ketogenic.http://www.ncbi.nlm.nih.gov/pubmed/19687389

"FACT: Calories neither determine weight OR body composition with certainty. Nigel / some CICO zealots may agree body composition changes are privy to nutrition, but wt is 100% controlled by calories. This is something they pretty much made up and biological science does not at all support this idea. Calories neither control body composition OR body weight/mass
with any certainty. The bulk consumed with fork and spoon does not need to stick on your body in the form of a mass laden tissue, ever."Calories determine weight change. See Bray et al shows that a calorie *is* a calorie (where weight change is concerned). It would have been nice if Fig. 6 had contained a plot of "Effect of energy intake on change in body weight", but it didn't.LBM = Lean Body MassFM = Fat Mass = Body FatWeight change = LBM change + FM change
Weight change varies from ~+3.5kg (@ +2,500kJ/d) to ~+9.1kg (@ +5,900kJ/d).
(Maximum weight increase)/(minimum weight increase) = 2.6
(Maximum kJ/day increase)/(minimum kJ/day increase) = 2.36∴ A calorie IS a calorie (where weight change is concerned).∴ Insufficient protein can result in loss of LBM (bad).

The main thrust of ItsTheWoo's argument is that inter-personal variations in weight gain from subject to subject, invalidates Bray's conclusion. It doesn't.
Some subjects become more energetic on a 40% caloric surplus, which increases their NEAT & TEA, which increases their Eout, which reduces their weight gain.
Some subjects don't change their energy on a 40% caloric surplus, which doesn't change their NEAT & TEA, which results in intermediate
weight gain.
Some subjects become less energetic on a 40% caloric surplus, which decreases their NEAT & TEA, which decreases their Eout, which increases their weight gain.

I believe that the Insulin Sensitivity (IS) of the subject determines which category they fall into and by how much. The higher the IS, the higher the energy, as high IS results in low serum insulin, which minimises sedation. Energy Balance always applies.

"Again, making crap up. There is NO RULE IN BIOLOGY which states all consumed energy must be retained as body mass. Indeed most typical people gain fat during overfeeding (with great resistance/inefficiency of fat gain), but it is indeed possible to hardly gain any or none at all as in constitutional thinness. What happens during calorie consumption among different people (and perhaps, different DIETS and different TIMES and different ENDOCRINE situations...) is a wild card determined by the biology i.e. neuroendocrine functions of the animal in question. There is NOTHING about physics which reflects / informs physiology other than the basic fact the latter
exists within the former (which, again, tells us NOTHING ultimately). How organisms process consumed nutrition is not a physics question. There is no freakin' law of physics or physiology for that matter which states nom nom time = thigh chub. You don't have to wear that pizza as a popeye's muscle or as a shelf butt."
Somewhere within all of the irrelevant waffle about rules & laws, ItsTheWoo raises an interesting point. Although a caloric surplus is always required for weight gain, eating more Calories can sometimes result in zero weight gain. How so? From ItsTheWoo's link:-
"Conclusion: This data is the first to demonstrate a resistance to weight gain in constitutional thinness (CT) population in response to 4-week fat overfeeding, associated with an increase in resting energy expenditure and an emphasised anorexigenic hormonal profile.
In CT people, their energy expenditure increases in line with their energy intake. Therefore, even though they're eating more Calories, there's no caloric surplus, therefore there's no weight gain. Energy Balance always applies.

"Yes, kcals do get wasted. You don't understand things quantitatively i.e. how many kcals get wasted."

"I know anxious/obsessional people like the safe feeling of balancing calories. The fact reality is more complex and you can't just enter things in a phone app and be ASSURED of what is going on in your body, doesn't invalidate the truth of the fact metabolic reactions are more complex THAN CALORIES.

Just because it is *impossible* for a reasonable free living human to quantify all of the metabolic, endocrine, nervous system factors influencing adipocyte growth changes does not mean they don't fucking exist."ItsTheWoo left out my calculations. Here they are:-"if I eat 2000 calories of a ketogenic diet in 3 hrs, most of it is wasted as heat, physical energy (I know, because I am EXTREMELY warm/energetic) and then the rest of time i am using a relatively greater percent of stored fat."
Do you know at what rate you're burning-off extra energy intake as heat energy output when you're "EXTREMELY warm/energetic"? Here's an estimate:-
If the mean TEF for your meal is 11% (assuming your meal is 50%E protein & 50%E fat), that's 220kcals (921kJ) "wasted" as heat energy. That'll make you feel EXTREMELY warm, as 220kcal raises the temperature of 57kg of water (your body) by 3.84°C.

A 2,000kcal meal (a whole day's worth of food) takes a lot longer than 3 hours to digest & absorb. I'll guesstimate it as 24 hours. 921kJ of extra heat power over the course of 24 hours = 10.7W, which is an increase of 17.7% over your normal Metabolic Rate of ~60W
heat power (~1kcal/minute).It's easy to "prove" something by being vague. That's PSEUDOSCIENCE. I do science. If you do the maths, you can see that, of the 2,000kcal ketogenic meal, most of it isn't wasted as heat, because if most of it is wasted as heat, ItsTheWoo would spontaneously combust!

"Dr. Robert C. Atkins made the same fundamental cock-up when he said that humans pissed-out loads of kcals of ketones each day, giving a Metabolic Advantage to ketogenic diets."

"1) The advantage of a ketogenic diet (non-fasting) does exist, so it's not a 'cock up", even if his mechanism was wrong.
2) If atkins was wrong (you pee out all LCHF food) who cares? That was 30+ years ago. He was a cardiologist who observed a VLC diet made him slim. He used his medical education to hypothesize a reason why. His hypothesis was wrong, but his observations were right. This happens all the time in science or basic human reasoning; make observations, form hypothesis. The hypothesis may be wrong, the findings are STILL RIGHT (i.e. low carb diets DO make slim, just not via peeing away ketones)."
1) There is no Metabolic Advantage to ketogenic diets. See http://www.jbc.org/content/92/3/679.full.pdf
2) Atkins' observations were wrong. See The Battle of the Diets: Is Anyone Winning (At Losing?)
a) Low-Carb diets work better than High-Carb diets for people who are Insulin Resistant.
b) Low-Carb diets work worse than High-Carb diets for people who are Insulin Sensitive.
c) Low-Carb diets work the same as High-Carb diets for everybody in Metabolic Ward Studies.
If there's a Metabolic Advantage to ketogenic diets, they would work better than high-carb diets all the time. They don't. See How low-carbohydrate diets result in more weight loss than high-carbohydrate diets for people with Insulin Resistance or Type 2 Diabetes for my hypothesis, which explains a), b) and c).

From the first link above:-
"Current ketogenic diets are all characterized by elevations of free fatty acids, which may lead to metabolic inefficiency by activation of the PPAR system and its associated uncoupling mitochondrial uncoupling proteins."

From the third link above:-
"Weight loss was similar between diets, but only the high-fat diet increased LDL-cholesterol concentrations. This effect was related to the lack of suppression of both fasting and 24-h FFAs."

EDIT: So much for fat being a "clean-burning" fuel for the heart. Some people believe that, because dietary fats pass from the small intestine, via the Lacteals, to circulation at the Subclavian vein, this means that the heart prefers to burn fatty acids.

All saturated fatty acids have a RR for CHD of 1.06 (95% CI 0.86 - 1.30).∴ There's no association between saturated fat intake and the RR for CHD.

Before VLC'ers do a dance of joy, consider the Forest plot for individual saturated fatty acids.Palmitic acid has a RR for CHD of 1.15 (95% CI 0.96 - 1.37).Stearic acid has a RR for CHD of 1.23 (95% CI 0.93 - 1.61).

Monday, 4 August 2014

Relating tissue HUFA balance with blood cholesterol and heart attacks.
Results from the 25-year follow-up in the Seven Countries Study [35] were discussed in an earlier review [10] which noted that “Food energy imbalances which elevate blood cholesterol may be fatal only to the degree that omega-6 (n-6) exceeds omega-3 (n-3) in tissue HUFA. Such evidence raises questions about the hypothesis that blood cholesterol levels cause CHD.”
Northern Europe and Southern Europe have abbreviations “No.” and “So.”,
respectively. The Figure is reprinted with permission of the publisher.

Fig. 1 is interesting, as it shows a significant association between 25-year CHD mortality and Serum Total Cholesterol for every region except Japan. What's different about Japan, compared to Northern Europe, USA, Serbia, Southern Europe & Crete?

"The link to the pathophysiology of depression is not clear. An overlooked connection is the role of magnesium, which acts as physiological NMDA-receptor antagonist:

1. There is overlap between the actions of ketamine with that of high doses of magnesium in animal models, finally leading to synaptic sprouting.

2.Magnesium and ketamine lead to synaptic strengthening, as measured by an increase in slow wave sleep in humans.

3.Pathophysiological mechanisms, which have been identified as risk factors for depression, lead to a reduction of (intracellular) magnesium. These are neuroendocrine changes (increased cortisol and aldosterone) and diabetes mellitus as well as Mg2+ deficiency.

6. Ketamine, directly or indirectly via non-NMDA glutamate receptor activation, acts to increase brain Mg2+ levels. Similar effects have been observed with other classes of antidepressants.

7.Depressed patients with low Mg2+ levels tend to be therapy refractory. Accordingly, administration of Mg2+ either alone or in combination with standard antidepressants acts synergistically on depression like behavior in animal models.

I'm wondering whether the amnesia for vivid dreams (if you wake up in the middle of one) is mediated by magnesium, as amnesia is a ketamine-like effect.

Therefore, a deficiency in magnesium may cause bad memories to linger, increasing the risk factor for situational depression.

4g/day of Epsom Salts provides 400mg/day of Magnesium. Dissolve the Epsom Salts in warm water and add the solution to your drinks over a 24 hour period, to maximise absorption & minimise laxation.

Friday, 1 August 2014

eA represents the amount of a substance that perturbs one of the body's negative feedback loops. The amount oscillates between 0V & 100V.

eR represents the effect of the substance on the body. 100V represents maximum effect and -100V represents maximum anti-effect.

The very first time that the substance is taken, there is 100V of effect, initially. As the time-constant of the negative feedback loop "kicks-in", the effect decays exponentially. Just before the substance is discontinued, the effect is down to 36.8V. Just after the substance is discontinued, the anti-effect is -63.2V. If the input continues to oscillate between 0V & 100V, the effect & anti-effect eventually become equal in magnitude. This is known as "cycling".

If the substance is applied continuously, theeffect decays exponentially to 0V. When the substance is discontinued, the anti-effect is -100V initially, but decays exponentially to0V.

This is analogous to drug tolerance, dependence & withdrawal, where eventually, the user has to take the drug just to feel normal, and discontinuing the drug gives the worst withdrawal symptoms ever, initially. After the drug has been discontinued for a while, the withdrawal symptoms decay exponentially to zero.

The above also applies to supplements that perturb one of the body's Hypothalamic Pituitary NFB loops e.g. the HPA (Adrenal), the HPG (Gonadal) or the HPT (Thyroid) Axes, or any other system (as everything in the body is regulated by a negative feedback loop).

This explains why a supplement can work really well at first, then its effect decays exponentially, until there is zero effect. The loop has compensated for it.

EDIT: If a loop is broken, due to zero secretion of one of the hormones controlling it, then a prescription drug/hormone restores the loop's output level to normal. E.g.

About Me

I have a B.Sc.(Hons) in Electronic Engineering but no qualifications in Diet, Nutrition & Fitness, which is why I back-up what I write with links to high-quality evidence.

You can email me at
nigel.kinbrum@entee'ellworld.com
(say it!).

My suggestions must ALWAYS be checked by your Pharmacist/GP first, in case of contraindications with other medical conditions or medications that I don't know about. My suggestions are adjuncts to, NOT replacements for medication(s).

If symptoms improve, ask your GP about a reduction in medication(s), if it's/they're causing you problems.

Cheers, Nigel Kinbrum B.Sc.(Hons)Eng.

Moderation Policy:-READ THIS BEFORE COMMENTING. I can approve comments using my phone when I'm away from my lap-top, but I prefer to type replies on my lap-top, so please be patient.

Competing Interest:- When you get a $5 discount by using code NIG935 on iHerb.com, I get a $5 reward.